Search results for "IMATINIB"

showing 10 items of 108 documents

Imatinib-Loaded Micelles of Hyaluronic Acid Derivatives for Potential Treatment of Neovascular Ocular Diseases

2018

In this work, new micellar systems able to cross corneal barrier and to improve the permeation of imatinib free base were prepared and characterized. HA-EDA-C-16, HA-EDA-C-16-PEG, and HA-EDA-C-16-CRN micelles were synthesized starting from hyaluronic acid (HA), ethylenediamine (EDA), hexadecyl chains (C-16), polyethylene glycol (PEG), or L-carnitine (CRN). These nanocarriers showed optimal particle size and mucoadhesive properties. Imatinib-loaded micelles were able to interact with corneal barrier and to promote imatinib transcorneal permeation and penetration. In addition, a study was conducted to understand the in vitro imatinib inhibitory effect on a choroidal neovascularization process…

0301 basic medicineCell SurvivalDrug CompoundingPharmaceutical ScienceAdministration Ophthalmic02 engineering and technologyPolyethylene glycolMicellePermeabilityCell LinePolyethylene GlycolsCornea03 medical and health scienceschemistry.chemical_compoundocular drug delivery hyaluronic acid polymeric micelles imatinib transcorneal permeation ocular neovascular diseasesCarnitinehemic and lymphatic diseasesDrug DiscoveryHyaluronic acidPEG ratiomedicineocular drug delivery; hyaluronic acid; polymeric micelles; imatinib; transcorneal permeation; ocular neovascular diseasesAnimalsHumansHyaluronic AcidParticle SizeProtein Kinase InhibitorsneoplasmsMicellesDrug CarriersEndothelial CellsImatinibPermeation021001 nanoscience & nanotechnologyEthylenediaminesIn vitroChoroidal NeovascularizationDrug Liberation030104 developmental biologychemistrySettore CHIM/09 - Farmaceutico Tecnologico ApplicativoBiophysicsImatinib MesylateMolecular Medicinelipids (amino acids peptides and proteins)CattleNanocarriers0210 nano-technologymedicine.drug
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Kinase Inhibitors in Multitargeted Cancer Therapy

2017

The old-fashioned anticancer approaches, aiming in arresting cancer cell proliferation interfering with non-specific targets (e.g. DNA), have been replaced, in the last decades, by more specific target oriented ones. Nonetheless, single-target approaches have not always led to optimal outcomes because, for its complexity, cancer needs to be tackled at various levels by modulation of several targets. Although at present, combinations of individual single-target drugs represent the most clinically practiced therapeutic approaches, the modulation of multiple proteins by a single drug, in accordance with the polypharmacological strategy, has become more and more appealing. In the perspective of…

0301 basic medicineDrugNiacinamideIndolesPyridinesmedia_common.quotation_subjectPharmacologyBioinformaticsBiochemistryReceptor tyrosine kinase03 medical and health sciencesCrizotinibPiperidinesMultitargeted drugs anticancer agents polypharmacology tyrosine kinase receptors oncogene addiction tumor microenvironment FDA-approved drugsNeoplasmsDrug DiscoverymedicineSunitinibHumansAnilidesPyrrolesProtein Kinase Inhibitorsmedia_commonPharmacologyTumor microenvironmentbiologybusiness.industryPhenylurea CompoundsOrganic ChemistryImidazolesCancerReceptor Protein-Tyrosine KinasesSorafenibmedicine.diseaseOncogene AddictionSettore CHIM/08 - Chimica FarmaceuticaClinical trialPyridazines030104 developmental biologyMechanism of actionbiology.proteinImatinib MesylateQuinazolinesMolecular MedicinePyrazolesmedicine.symptombusinessTyrosine kinase
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Imatinib spares cKit-expressing prostate neuroendocrine tumors, whereas kills seminal vesicle epithelial-stromal tumors by targeting PDGFR-β

2017

Abstract Prostate cancer is a leading cause of cancer-related death in males worldwide. Indeed, advanced and metastatic disease characterized by androgen resistance and often associated with neuroendocrine (NE) differentiation remains incurable. Using the spontaneous prostate cancer TRAMP model, we have shown that mast cells (MCs) support in vivo the growth of prostate adenocarcinoma, whereas their genetic or pharmacologic targeting favors prostate NE cancer arousal. Aiming at simultaneously targeting prostate NE tumor cells and MCs, both expressing the cKit tyrosine kinase receptor, we have tested the therapeutic effect of imatinib in TRAMP mice. Imatinib-treated TRAMP mice experience a pa…

0301 basic medicineMaleCancer ResearchReceptor tyrosine kinaseAntineoplastic AgentProstate cancerMice0302 clinical medicineProstatebiologySeminal VesiclesImmunohistochemistryGene Expression Regulation NeoplasticNeuroendocrine TumorsProto-Oncogene Proteins c-kitmedicine.anatomical_structureOncology030220 oncology & carcinogenesisImatinib MesylateFemaleNeuroendocrine Tumormedicine.drugTrampHumanSignal TransductionPCA3medicine.medical_specialtyStromal cellXenograft Model Antitumor AssayProtein Kinase InhibitorAntineoplastic AgentsMice TransgenicReceptor Platelet-Derived Growth Factor beta03 medical and health sciencesInternal medicineSeminal VesiclemedicineAnimalsHumansProtein Kinase InhibitorsAnimalProstatic NeoplasmsImatinibBiomarkermedicine.diseaseXenograft Model Antitumor AssaysDisease Models Animal030104 developmental biologyEndocrinologyImatinib mesylateProstatic Neoplasmbiology.proteinCancer researchBiomarkers
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Interleukin 3- receptor targeted exosomes inhibit in vitro and in vivo chronic myelogenous Leukemia cell growth

2017

Despite Imatinib (IM), a selective inhibitor of Bcr-Abl, having led to improved prognosis in Chronic Myeloid Leukemia (CML) patients, acquired resistance and long-term adverse effects is still being encountered. There is, therefore, urgent need to develop alternative strategies to overcome drug resistance. According to the molecules expressed on their surface, exosomes can target specific cells. Exosomes can also be loaded with a variety of molecules, thereby acting as a vehicle for the delivery of therapeutic agents. In this study, we engineered HEK293T cells to express the exosomal protein Lamp2b, fused to a fragment of Interleukin 3 (IL3). The IL3 receptor (IL3-R) is overexpressed in CML…

0301 basic medicineMedicine (miscellaneous)PharmacologyEngineered exosomeExosomesInterleukin 3Antineoplastic AgentMiceHEK293 Cellhemic and lymphatic diseasesDrug CarrierPharmacology Toxicology and Pharmaceutics (miscellaneous)Drug CarriersChronic myeloid leukemiaMyeloid leukemiaChronic myeloid leukemia; Drug delivery; Drug resistance; Engineered exosomes; Interleukin 3; Animals; Antineoplastic Agents; Cell Line Tumor; Cell Proliferation; Disease Models Animal; Drug Carriers; Exosomes; HEK293 Cells; Heterografts; Humans; Imatinib Mesylate; Leukemia Myelogenous Chronic BCR-ABL Positive; Mice; Receptors Interleukin-3; Treatment Outcome3. Good healthTreatment OutcomeImatinib MesylateHeterograftsHeterograftResearch Papermedicine.drugHumanEngineered exosomesAntineoplastic Agents03 medical and health sciencesIn vivoCell Line TumorLeukemia Myelogenous Chronic BCR-ABL PositivemedicineAnimalsHumansneoplasmsInterleukin 3.Interleukin 3Cell Proliferationbusiness.industryAnimalImatinibmedicine.diseaseMicrovesiclesReceptors Interleukin-3ExosomeDisease Models AnimalHEK293 Cells030104 developmental biologyImatinib mesylateDrug resistanceCancer cellDrug deliverybusinessChronic myelogenous leukemia
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BCR-ABL1 Doubling-Times and Halving-Times May Predict CML Response to Tyrosine Kinase Inhibitors

2019

In Chronic Myeloid Leukemia (CML), successful treatment requires accurate molecular monitoring to evaluate disease response and provide timely interventions for patients failing to achieve the desired outcomes. We wanted to determine whether measuring BCR-ABL1 mRNA doubling-times (DTs) could distinguish inconsequential rises in the oncogene’s expression from resistance to tyrosine kinase inhibitors (TKIs). Thus, we retrospectively examined BCR-ABL1 evolution in 305 chronic-phase CML patients receiving imatinib mesylate (IM) as a first line treatment. Patients were subdivided in two groups: those with a confirmed rise in BCR-ABL1 transcripts without MR3.0 loss and those failing IM. We found …

0301 basic medicineOncologyCancer Researchmedicine.medical_specialtyDisease ResponseChronic Myeloid LeukemiaBCR-ABL1/ABL1IShalving-timelcsh:RC254-28203 medical and health sciences0302 clinical medicineInternal medicinehemic and lymphatic diseasesBCR-ABL1/ABL1; IS; Chronic Myeloid Leukemia; Doubling-time; Halving-time; Tyrosine kinase inhibitorstyrosine kinase inhibitorsmedicineDoubling timeOriginal ResearchBCR-ABL1/ABL1Oncogenebusiness.industryMyeloid leukemialcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensDiscontinuationdoubling-time030104 developmental biologyImatinib mesylateOncology030220 oncology & carcinogenesisCohortISBCR-ABL1/ABL1 ISbusinessTyrosine kinaseFrontiers in Oncology
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High BCR-ABL/GUS(IS) levels at diagnosis of chronic phase CML are associated with unfavorable responses to standard-dose imatinib

2017

Abstract Purpose: The approval of second-generation tyrosine kinase inhibitors (TKIs) for the first-line treatment of chronic myeloid leukemia (CML) has generated an unmet need for baseline molecular parameters associated with inadequate imatinib responses. Experimental Design: We correlated BCR–ABL/GUSIS and BCR–ABL/ABL transcripts at diagnosis with the outcome—defined by the 2013 European LeukemiaNet recommendations—of 272 patients newly diagnosed with CML receiving imatinib 400 mg/daily. Applying receiver-operating characteristic curves, we defined BCR–ABL/GUSIS and BCR–ABL/ABL levels associated with lower probabilities of optimal response, failure-free (FFS), event-free (EFS), transform…

0301 basic medicineOncologyCancer Researchmedicine.medical_specialtyPathologyMyeloidBCR-ABL Diagnosis CMLDrug intolerance03 medical and health sciences0302 clinical medicinehemic and lymphatic diseasesInternal medicineDiagnosismedicineBCR-ABLCMLneoplasmsABLbusiness.industryCancerMyeloid leukemiaImatinibOncology cancer researchmedicine.diseaseLeukemia030104 developmental biologymedicine.anatomical_structureOncology030220 oncology & carcinogenesisbusinessTyrosine kinasemedicine.drug
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Type and gene location of kit mutations predict progression-free survival to first-line imatinib in gastrointestinal stromal tumors: A look into the …

2021

In previous studies on localized GISTs, KIT exon 11 deletions and mutations involving codons 557/558 showed an adverse prognostic influence on recurrence-free survival. In the metastatic setting, there are limited data on how mutation type and codon location might contribute to progression-free survival (PFS) variability to first-line imatinib treatment. We analyzed the type and gene location of KIT and PDGFRA mutations for 206 patients from a GIST System database prospectively collected at an Italian reference center between January 2005 and September 2020. By describing the mutational landscape, we focused on clinicopathological characteristics according to the critical mutations and inve…

0301 basic medicineOncologyCancer Researchmedicine.medical_specialtyStromal cellPDGFRAlcsh:RC254-28203 medical and health sciencesExon0302 clinical medicinePredictive biomarkersInternal medicineGene duplicationmedicineGastrointestinal stromal tumorsProgression-free survivalGeneneoplasmsGiSTbusiness.industryImatinibKITlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens030104 developmental biologyOncology030220 oncology & carcinogenesisImatinibbusinessMutationsmedicine.drugGIST
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Intermittent targeted therapies and stochastic evolution in patients affected by chronic myeloid leukemia

2016

Front line therapy for the treatment of patients affected by chronic myeloid leukemia (CML) is based on the administration of tyrosine kinase inhibitors, namely imatinib or, more recently, axitinib. Although imatinib is highly effective and represents an example of a successful molecular targeted therapy, the appearance of resistance is observed in a proportion of patients, especially those in advanced stages. In this work, we investigate the appearance of resistance in patients affected by CML, by modeling the evolutionary dynamics of cancerous cell populations in a simulated patient treated by an intermittent targeted therapy. We simulate, with the Monte Carlo method, the stochastic evolu…

0301 basic medicineOncologyDrugStatistics and Probabilitymedicine.medical_specialtymedicine.medical_treatmentmedia_common.quotation_subjectTargeted therapy03 medical and health sciencesClassical Monte Carlo simulations; computational biology; models for evolution (theory); mutational and evolutionary processes (theory); Statistical and Nonlinear Physics; Statistics and Probability; Statistics Probability and Uncertainty0302 clinical medicinecomputational biologyInternal medicinemedicineClassical Monte Carlo simulationmutational and evolutionary processes (theory)media_commonbusiness.industryMyeloid leukemiaStatistical and Nonlinear PhysicsImatinibSettore FIS/07 - Fisica Applicata(Beni Culturali Ambientali Biol.e Medicin)Axitinib030104 developmental biology030220 oncology & carcinogenesisCancer cellToxicityStatistics Probability and Uncertaintybusinessmodels for evolution (theory)Tyrosine kinasemedicine.drugStatistical and Nonlinear Physic
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Imatinib rechallenge in patients with advanced gastrointestinal stromal tumors following progression with imatinib, sunitinib and regorafenib

2018

Background: Rechallenge with imatinib is an option in advanced gastrointestinal stromal tumor (GIST) patients following progression with standard tyrosine-kinase inhibitors (TKIs), imatinib, sunitinib and regorafenib. We retrospectively collected data from metastatic Italian GIST patients treated with imatinib resumption after progression to conventional TKIs. Methods: A total of 104 eligible advanced GIST patients, previously treated with imatinib, sunitinib and regorafenib, were collected from six referral Italian institutions. Mutational analysis was recorded and correlated with survival and response according to RECIST 1.1 or CHOI criteria. Results: Overall, 71 patients treated with ima…

0301 basic medicineOncologymedicine.medical_specialtyStromal cellrechallengelcsh:RC254-28203 medical and health scienceschemistry.chemical_compound0302 clinical medicineInternal medicineRegorafenibhemic and lymphatic diseasesmedicineIn patientStromal tumorneoplasmsOriginal ResearchGiSTbusiness.industrySunitinibImatiniblcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensexon 11 KIT mutationTKI030104 developmental biologyOncologychemistryexon 11 KIT mutation; GIST; imatinib; rechallenge; TKIimatinib030220 oncology & carcinogenesisbusinessGIST; TKI; exon 11 KIT mutation; imatinib; rechallengemedicine.drugGIST
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SWATH-MS based quantitative proteomics analysis reveals that curcumin alters the metabolic enzyme profile of CML cells by affecting the activity of m…

2018

Background Chronic myelogenous leukemia (CML) is a myeloproliferative disorder caused by expression of the chimeric BCR-ABL tyrosine kinase oncogene, resulting from the t(9;22) chromosomal translocation. Imatinib (gleevec, STI-571) is a selective inhibitor of BCR-ABL activity highly effective in the treatment of CML. However, even though almost all CML patients respond to treatment with imatinib or third generation inhibitors, these drugs are not curative and need to be taken indefinitely or until patients become resistant. Therefore, to get a definitive eradication of leukemic cells, it is necessary to find novel therapeutic combinations, for achieving greater efficacy and fewer side effec…

0301 basic medicineProteomicsCancer ResearchCurcuminCML cellsCellReceptors Cytoplasmic and NuclearKaryopherinsTransfectionlcsh:RC254-282Mass SpectrometrymiR-22/IPO7/HIF-1α axis03 medical and health scienceschemistry.chemical_compound0302 clinical medicinemiR-22/IPO7/HIF-1α axiSettore BIO/13 - Biologia Applicatahemic and lymphatic diseasesCell Line TumorLeukemia Myelogenous Chronic BCR-ABL PositivemedicineHumansCML cells; Curcumin; miR-22/IPO7/HIF-1α axis; SWATH-MS; Oncology; Cancer ResearchOncogeneChemistryResearchCML cellImatinibTransfectionmedicine.diseaseHypoxia-Inducible Factor 1 alpha Subunitlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens3. Good healthMicroRNAs030104 developmental biologymedicine.anatomical_structureOncology030220 oncology & carcinogenesisCancer researchCurcuminSWATH-MSK562 CellsTyrosine kinaseK562 cellsChronic myelogenous leukemiamedicine.drug
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